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(Hypertension. 2005;46:271.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

The Many Possible Benefits of Natriuretic Peptides After Myocardial Infarction

From the Experimental Cardiovascular Biology Research Unit, Institut de Recherches Cliniques de Montréal (IRCM), Montreal, Quebec, Canada.

Correspondence to Christian F. Deschepper, IRCM, 110 Pine Ave W, Montréal, Quebec, Canada H2W 1R7. E-mail christian.deschepper@ircm.qc.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Natriuretic peptides (NPs) are well-known markers of the ventricular hypertrophic response, as documented in many studies performed either in animals or with cultured cardiomyocytes. In recent years, evidence has been mounting that NPs are in fact negative regulators of the hypertrophic response, as reviewed recently.¹ In this light, NPs appear as endogenous cardioprotective agents of which expression increases in reaction to myocardial pathological conditions, but it is still unclear to which extent these agents may actually decrease mortality. In this issue of Hypertension, Nakanashi et al² show that when myocardial infarction (MI) is induced by permanent occlusion of the coronary artery, mortality by heart failure is increased in knockout mice with inactivation of the gene coding for the NP receptor guanylyl cyclase-A (GC-A). Beyond these short-term effects, inactivation of GC-A also worsens post-MI chronic ventricular remodeling. Although the present study does not show whether these chronic remodeling processes also increase mortality at a later stage, the remodeling is accompanied by ventricular enlargement and decreased fractional shortening, both of which usually associate with poor prognosis. The importance of these data is enhanced by the fact that increasing numbers of studies are investigating the utility of recombinant NPs in humans.³ However, several questions remain concerning the particular modes of action of NPs.

One issue concerns the question of whether NPs work via peripheral mechanisms or via a direct action on the myocardium. Importantly, congestive heart failure is accompanied by volume expansion, and the present article shows that the natriuresis and diuresis . . . [Full Text of this Article]

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